Evidence map›Paper›PMID 35204666›Full record

ArticleBiomolecules2022

Recent Advances in Our Molecular and Mechanistic Understanding of Misfolded Cellular Proteins in Alzheimer's Disease (AD) and Prion Disease (PrD).

Walter J Lukiw

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 18 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Walter J LukiwDepartments of Neurology, Neuroscience and Ophthalmology, LSU Neuroscience Center, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
Louisiana State University Health Sciences Center New Orleans · US

Funding

microRNA (miRNA) signaling in Alzheimer's disease(AD)R01AG038834 · NIA · LSU HEALTH SCIENCES CENTER · PI BAZAN, NICOLAS G. · 2011 to 2020
$3.3M
Gene Expression in Alzheimer's DiseaseR01AG018031 · NIA · LSU HEALTH SCIENCES CENTER · PI LUKIW, WALTER J · 2001 to 2006
$1.4M
National Institute of Health NEI EY006311NIH HHS AG038834NIH HHS NIA AG18031
6 · The paper itself

Abstract

Naturally occurring neuron-abundant proteins including amyloid Aβ42 peptide and the microtubule-associated protein tau (MAPT) can, over time and under pathological situations, assume atypical conformations, altering their normal biological structure and function, and causing them to aggregate into insoluble and neurotoxic intracellular inclusions. These misfolded proteins ultimately contribute to the pathogenesis of several progressive, age-related and ultimately lethal human neurodegenerative disorders. The molecular mechanism of this pathological phenomenon of neuronal protein misfolding lends support to the '

Indexed as

Alzheimer DiseaseCreutzfeldt-Jakob SyndromePrion DiseasesPrionsScrapieAnimalsHumansSheepPrionsAlzheimer’s disease (AD)atypical protein foldingfrontotemporal degeneration (FTD)prion disease (PrD)proteostasistauopathies

Identifiers

PMID35204666
PMCPMC8961532
OpenAlexW4207038655

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.